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PubMed2003

[Remodeling of coronary arteries examined by arteries intravascular ultrasonography].

UNLABELLED: In most papers atherosclerotic remodelling was assessed in one segment of each studied artery. Such mode of study makes impossible to investigate the homogeneity of the remodelling. The aim of the study was intravital assessment by means of intravascular ultrasonography (IVUS) of the incidence of positive and negative remodelling in coronary artery segments and verification of the hypothesis that remodelling is inhomogeneous within the same artery. METHOD: Remodelling was assessed quantitatively by IVUS (3.5 F; 20 MHz Visions Five-64 F/X catheters, Oracle In-Vision Imaging System, Endosonics Corp. USA) in 48 segments of 27 coronary arteries. On the base of the difference between total vessel area (TA) at lesion site and reference cross-section (plaque area < 35%) remodelling was classified as negative, positive or absent. In 13 arteries out of 27 studied arteries more than 1 segment was assessed, containing both cross-section with > 50% stenosis and reference cross-section. RESULTS: Positive, negative and absent remodelling was observed in 54%, 29% and 17% of segments, respectively. The analysis revealed two different types of remodelling in 7 out of 13 arteries with several analysed segments. This finding demonstrates that remodelling is inhomogenous within the artery (p < 0.006). CONCLUSIONS: Compensatory enlargement is the most common response of coronary arteries to atherosclerotic plaque development followed by negative remodelling and absence of remodelling. Not homogenous remodelling within the same artery suggests a prominent role of local factors in determining the type of response of the artery to plaque accumulation.

Adult↗

PubMed1999

Predictors of early and late ventricular remodeling after acute myocardial infarction.

BACKGROUND: The determinants of the early and late stages of the ventricular remodeling process after infarction are not well defined. HYPOTHESIS: The study was undertaken to evaluate the factors that condition the time course of left ventricular dilation during the first 6 months after infarction. METHODS: The study group consisted of 74 patients with a first intermediate-large (> or = 4 Q waves) acute myocardial infarction. Contrast left ventricular and coronary angiograms were performed at 7 +/- 1 and 175 +/- 25 days after infarction. Left ventricular volumes, regional function and infarction artery status were quantified. Percutaneous transluminal coronary angioplasty (PTCA) was performed in the early angiogram in 31 patients. RESULTS: In the early angiogram, 13 patients showed ventricular remodeling (end-diastolic volume > 90 ml/m2). A larger extent of dysfunction was the only predictor (p < 0.002) of early remodeling. At 6 months, a smaller, early end-diastolic volume (p < 0.0001) and a poorer regional function recovery (p < 0.05) were independently related to late diastolic enlargement, and a poorer regional function recovery (p < 0.0001) and a smaller, early end-systolic volume (p < 0.009) were independently related to late systolic enlargement. One patient with compared with 20 patients without early remodeling (p < 0.04) presented with late remodeling (increment of the end-diastolic volume > 20% at 6 months). In patients with early remodeling, the end-diastolic volume did not change significantly (101 +/- 13 vs. 94 +/- 22 ml/m2, NS) at 6 months; despite this, they maintained larger diastolic volumes than patients with late remodeling (81 +/- 12 ml/m2, p < 0.04) at 6 months. Infarction artery status did not influence the evolution of ventricular volumes and regional function. CONCLUSIONS: (1) A large infarct size is the main determinant of postinfarction remodeling. (2) Such infarct size-dependent ventricular dilation occurs early and does not tend to increase in late stage; in contrast, some cases of intermediate-large size infarcts without early remodeling exhibit late remodeling associated with a poor late recovery of regional function. (3) Recovery of regional function (indicating myocardial viability) rather than infarction artery status plays a role in the late ventricular remodeling process.

Aged↗

PubMed2002

Relation between left ventricular remodeling and clinical outcomes in heart failure patients with left ventricular systolic dysfunction.

BACKGROUND: A major advance in understanding the pathophysiology of the heart failure syndrome has been an understanding of the process of left ventricular (LV) remodeling. After any insult to the left ventricle resulting in diminished systolic performance and stroke volume, a series of histopathologic changes in the myocardium and structural changes in the LV chamber occurs over time. METHODS AND RESULTS: Early work on understanding this process of LV remodeling emerged from the studies of Pfeffer and colleagues, who used a rat model of myocardial infarction (MI). Compared to those with smaller MIs, rats with larger induced MIs underwent a substantially greater degree of chamber remodeling over time, and importantly, these structural changes were associated with significantly higher morality. These studies established for the first time the relation between the structural changes now widely known as LV remodeling and a natural history outcome in the setting of LV systolic dysfunction. Subsequently, these investigators demonstrated that angiotensin-converting enzyme (ACE) inhibition with captopril, when initiated soon after the induced MI, attenuated the remodeling process. Also observed was an improvement in survival among rats in whom the remodeling process has been attenuated. These important data paved the way for human studies that have subsequently provided substantial evidence to support two important concepts: (1) that LV remodeling is related to clinical outcomes that represent the natural history of the heart failure syndrome such as mortality and surrogate markers of the progression of heart failure, and (2) that therapeutic interventions in humans that slow or reverse the process of LV remodeling, such as ACE inhibitors and beta-blockers, appear to have a favorable effect on that natural history. CONCLUSIONS: This review will examine the issue of the relation between LV remodeling and clinical outcomes in the human heart failure syndrome from several interrelated aspects: (1) the relation between LV volume at one time point and subsequent oucome, (2) the relation between changes in LV volumes over time (LV remodeling) and clinical outcomes, and (3) the relation between the effect of medical therapeutic interventions on the LV remodeling process and the effect of those same medical interventions on natural history outcomes in human heart failure.

Adrenergic beta-Antagonists↗

PubMed2001

Bisphosphonate treatment suppresses not only stochastic remodeling but also the targeted repair of microdamage.

Two kinds of remodeling, stochastic and targeted, have been proposed based on the observation that microdamage in bone can initiate the remodeling process. Bisphosphonates are known to suppress stochastic bone remodeling. It has been hypothesized that bisphosphonates allow microdamage to accumulate, suggesting that they also suppress targeted remodeling. This study investigated whether suppression of remodeling using bisphosphonates inhibits remodeling targeted to repair microdamage, or whether the suppression of stochastic remodeling alone can account for the observed increase in damage accumulation. Beagle dogs were divided into three groups: control (CNT), risedronate-treated (RIS), and alendronate (ALN)-treated groups. The doses of both bisphosphonates were 6 times higher than the clinical doses. After 1-year treatment, animals were sacrificed and the right 9th rib was assigned to microdamage analysis. There were 3.06 times more associations between cracks and resorption spaces in CNT than expected (P < 0.005), indicating that remodeling normally targets cracks for repair, i.e., cracks can initiate a new remodeling event. However, although there was increased microdamage accumulation in RIS and ALN compared with CNT, fewer cracks than expected were associated with resorption spaces. The observation in RIS and ALN that there were fewer associations between cracks and resorption spaces than expected indicates that both targeted and non-targeted remodeling are suppressed in these groups. These data further suggest that the complete suppression of targeted remodeling could account for the increased microdamage burden.

Alendronate↗

PubMed2003

Preintervention arterial remodeling affects vessel stretch and plaque extrusion during coronary stent deployment as demonstrated by three-dimensional intravascular ultrasound.

The mechanisms of lumen enlargement during stent implantation may be significantly affected by arterial remodeling. To assess effects of lesion remodeling, we performed 3-dimensional intravascular ultrasound (IVUS) analyses in 55 coronary lesions before and after deployment of balloon-expandable stents. Standard quantitative analysis was performed, and arterial remodeling was assessed by the remodeling index (target site divided by mean of proximal and distal reference segment vessel areas), which classified lesions into group A (remodeling index < or =1, negative or intermediate remodeling, n = 40) or group B (remodeling index >1, positive remodeling, n = 15) lesions. Characteristics of the 55 patients and the interventional procedures were similar in the 2 groups. IVUS demonstrated that stenting resulted in increased lumen and vessel dimensions and in a reduced plaque size (p < or =0.001 each) in both group A and group B lesions. The extent of lumen increase inside the stents was almost identical, but resulted from different mechanisms: (1) vessel stretch was greater in group A (p <0.002 at minimum lumen site); (2) plaque compression (or embolization) tended to be greater in group B (p = 0.05, along entire stented segment); (3) plaque redistribution within the stent was observed in both groups (p <0.005 both); and (4) significant (p <0.01) plaque extrusion into the distal reference segment was found in group B only. Thus, the remodeling pattern of coronary lesions has a significant impact on the mechanisms of lumen enlargement during stent deployment. Lesions with positive remodeling show more plaque extrusion into the distal reference and less stent-induced vessel stretch than those with negative remodeling.

Aged↗

PubMed2000

Arterial remodeling in atherosclerosis, restenosis and after alteration of blood flow: potential mechanisms and clinical implications.

Arterial remodeling is currently being recognized as an important determinant in vascular pathology in which narrowing of the lumen is the predominant feature. Not only expansive remodeling (enlargement), but also constrictive remodeling (shrinkage) is observed in de novo atherosclerosis, in restenosis and in transplant vasculopathy. Expansive remodeling prevents and constrictive remodeling enhances luminal narrowing by plaque formation or intimal hyperplasia. The mechanisms of the opposite remodeling modes is unknown. Insight into the processes that determine the direction of local arterial remodeling may help to develop new strategies to prevent arterial occlusive disease. In the present paper the current status of research in the field of arterial remodeling in cardiovascular disease is reviewed. Mechanisms of arterial remodeling, potential interventions to influence the mode of remodeling as well as the methodological limitations of remodeling studies are discussed.

Angioplasty, Balloon↗

PubMed1999

Preintervention arterial remodeling as an independent predictor of target-lesion revascularization after nonstent coronary intervention: an analysis of 777 lesions with intravascular ultrasound imaging.

BACKGROUND: Pathological and intravascular ultrasound (IVUS) studies have documented arterial remodeling during atherogenesis. However, the impact of this remodeling process on the long-term outcome after percutaneous intervention is unknown. METHODS AND RESULTS: We used preintervention IVUS to define positive and negative/intermediate remodeling in a total of 777 lesions in 715 patients treated with nonstent techniques. Positive remodeling (lesion external elastic membrane area greater than average reference) was present in 313 lesions; intermediate/negative remodeling (lesion external elastic membrane area less than or equal to reference) was present in the other 464. Baseline clinical and angiographic characteristics were similar, except for a slightly higher percentage of insulin-dependent diabetic patients (10.2% versus 6.1%; P=0.054) in the negative/intermediate-remodeling group. Angiographic success and in-hospital and short-term complications were comparable in the 2 groups. There was no significant correlation between remodeling (as a continuous variable) and final lumen area (r=0.06) or final lesion plaque burden (r=0.17). At 18+/-13 months of clinical follow-up, both groups had similar rates of death and Q-wave myocardial infarction: 3.4% and 2.5% for the negative/intermediate-remodeling group versus 2.7% and 2.7% for the positive-remodeling group. However, the target-lesion revascularization (TLR) rate was 20.2% for the negative/intermediate-remodeling group versus 31.2% for the positive-remodeling group (P=0.007), and remodeling, as a continuous variable, was strongly correlated with probability of TLR (P=0.0001). By multivariable logistic regression analysis, diabetes (OR=2.3), left anterior descending artery location (OR=1.8), and remodeling (OR=5.9) were independent predictors of TLR. CONCLUSIONS: Positive lesion-site remodeling is associated with a higher long-term TLR after a nonstent interventional procedure. Thus, long-term clinical outcome appears to be determined in part by preintervention lesion characteristics.

Aged↗

PubMed1992

Periosteal and endosteal control of bone remodeling under torsional loading.

The shape changes that occur in the mid-diaphysis of a long bone due to adaptive remodeling induced by increasing or decreasing the axial and/or torsional loading of the bone are investigated using a simple model. In this model the mid-diaphysis of a long bone is represented as a hollow thick-walled right-circular cylinder, and different optimal strategies for bone remodeling are considered. It is shown that if such a thick-walled right-circular cylinder capable of surface remodeling is subjected to an axial compressive load and a twisting torque, then the remodeling patterns depend on whether the periosteal surface or the endosteal surface controls the limits of the remodeling process. It is shown that the effect of increasing the torque is always opposite to the effect of increasing the compressive load. Thus, similar remodeling patterns are obtained by increasing one type of loading and decreasing the other. Aside from the restriction of idealized cylindrical geometry, the only assumptions made are that the bone tissue is linearly elastic and that there exists a finite range of remodeling equilibrium stresses. Only those loading situations which maintain the bone in remodeling equilibrium are considered in this work. It follows that the results presented are independent of the specific type of rule governing the temporal evolution of the bone shape, since any such rule applies only in situations where there is active remodeling and, hence, no remodeling equilibrium.

Biomechanical Phenomena↗

PubMed1999

Dobutamine stress echocardiography predicts left ventricular remodeling after acute myocardial infarction.

BACKGROUND AND OBJECTIVES: Left ventricular (LV) remodeling after acute myocardial infarction (MI) is strongly related to infarct size. The contribution of viability in the infarct zone and the presence of multivessel disease remains unknown. Because dobutamine stress echocardiography (DSE) can estimate infarct size and detect myocardial viability and multivessel disease, we postulated that DSE can accurately predict LV remodeling after acute MI. METHODS: To test this hypothesis, 30 patients age 59 +/- 15 years, 21 men, 14 with anterior MI, underwent multistage DSE (low dose, 5 to 10 microg, and peak dose) during the first week after MI occurred. Follow-up echocardiography was performed at >/=1 year. LV remodeling (2 SD increase in LV volume) occurred in 17 of 30 patients. Remodeling occurred in 12 (92%) of 13 patients with large nonviable infarct and in 1 (13%) of 8 patients with large viable infarct (P <.001). Univariate predictors of LV remodeling were baseline ejection infarct (P <.01), infarct size (number of akinetic segments at low dose P <.01), age (P <.05), and multivessel coronary disease (P <. 01). The only multivariate predictor of remodeling was infarct size. Viability of infarct zone was a negative predictor of LV remodeling. CONCLUSION: DSE performed during the first week after acute MI predicts subsequent LV remodeling. Infarct size, nonviability of the infarct zone, and age are independent predictors of LV remodeling. Myocardial viability is a strong negative predictor of LV remodeling.

Adult↗

PubMed2003

Transmural action potential changes underlying ventricular electrical remodeling.

INTRODUCTION: Although it is well established that alterations in heart rate or activation sequence induce electrical remodeling in the atria, electrical remodeling in the ventricle is poorly understood. METHODS AND RESULTS: To determine the changes in cellular repolarization that underlie ventricular electrical remodeling caused separately by altered heart rate and activation sequence, optical action potentials were recorded simultaneously from 256 sites spanning the transmural wall of the arterially perfused canine wedge preparation (n = 15). Action potentials were compared from the same sites under identical conditions [endocardial pacing, cycle length (CL) = 1,000 msec], before and after an intervening 20- to 60-minute period of remodeling induced by (1) rapid pacing (CL = 300 msec) with no change in activation sequence; (2) altered activation sequence (epicardial pacing) with no change in rate; or (3) no change in rate or activation sequence (control). Action potential duration (APD) shortened by 24.8 +/- 4.8 msec following a period of rapid heart rate (P < 0.05) but prolonged (by 12.7 +/- 1.8 msec) following a period of altered activation sequence (P < 0.05). Hence, even after restoration of baseline heart rate and activation sequence, there were persistent changes in APD from baseline, indicative of electrical remodeling. Moreover, the orientation of the maximum APD gradient across the transmural wall changed more significantly following heart rate remodeling (by 27.7 degrees +/- 4.9 degrees, P < 0.05) than following activation sequence remodeling (by 12.3 degrees +/- 2.4 degrees, P < 0.05). CONCLUSION: Persistent changes in ventricular repolarization can be induced by surprisingly short periods of altered rate or activation sequence. In contrast to atrial remodeling, electrical remodeling in the ventricle can result in prolonged APD (with altered activation sequence) or reversal of APD gradient orientation (with rapid rate), suggesting that the nature of ventricular electrical remodeling induced by these two perturbations is different.

Action Potentials↗

PubMed1982

Cellular kinetics of the bone remodeling sequence in the rat.

The kinetics of the bone remodeling sequence in the rat has been studied using a system in which well-synchronized remodeling units were induced along the periosteum of rat mandibles. Remodeling of the periosteal surface of the mandibles was induced according to Tran Van (1979) by extraction of the opposing row of teeth; namely, the right maxillary molars were extracted under light ether anesthesia, therefore allowing the right mandibular molars to egress; this, in turn, induced a wave of remodeling activity on the buccal side of the periosteal surface of the alveolar bone. The quantification of the different cellular activities involved in bone remodeling has been performed up to 16 days after induction. This allowed us to demonstrate the sequential activity of the different cell types involved in bone remodeling, to study the cellular kinetics of this sequence of events, and to directly measure the duration of each phase of the bone remodeling sequence. A single wave of osteoclasts appeared 3 days after induction, reached a peak of 4-5 days, and then decreased sharply. This was followed by a single wave of mononuclear cells (Baron et al., 1980) within remodeling sites during the reversal phase; they appeared 4 days after induction, reached a peak by day 7, and then decreased sharply. This reversal activity was then followed by osteoblasts forming new bone on top of a reversal cement line in the remodeling sites, starting 6 days after induction and increasing until the end of the experiment. In addition, the synchronization of the system used in this study allowed direct measurement of the duration of the successive steps of the remodeling sequence. The directly measured values have then been compared to previous data calculated from other systems.

Animals↗

PubMed2026

Coordinated inflammatory macrophage and vascular smooth muscle cell remodeling signatures in human atherosclerosis: An integrative single-cell and bulk transcriptomic analysis.

Atherosclerotic plaque progression is shaped by coordinated inflammatory and remodeling programs involving immune cells and vascular wall cells. Inflammatory macrophage activation and vascular smooth muscle cell (VSMC) phenotypic remodeling are central features of human atherosclerosis, but their transcriptomic relationships during plaque progression remain incompletely characterized. This study integrated single-cell and bulk transcriptomic datasets to examine highly inflammatory macrophage states, VSMC remodeling-related transcriptional programs, and candidate ligand-receptor expression patterns in human atherosclerotic plaques. Human atherosclerotic plaque single-cell RNA sequencing data from GSE260657 and bulk transcriptomic data from GSE28829 were analyzed. After quality control, 7628 cells were retained for single-cell analysis. Major cell types were annotated using canonical markers, followed by reclustering of macrophages and VSMC-related cells. Functional module scoring, differential expression analysis, Gene Ontology biological process enrichment, and Kyoto Encyclopedia of Genes and Genomes pathway analyses were performed to characterize macrophage transcriptional states. Slingshot was applied to infer VSMC pseudotime ordering. CellChat and NicheNet were used to prioritize candidate ligand-receptor expression patterns and ligand-associated VSMC target gene programs. External bulk transcriptomic analysis was performed to examine whether single-cell-derived inflammatory and remodeling signatures were represented at the tissue-transcriptome level during plaque progression. Macrophage reclustering identified a highly inflammatory macrophage state characterized by prominent inflammatory activation, cytokine-response, and stress-response features. Genes upregulated in this population were enriched in pathways related to tumor necrosis factor (TNF) response, nuclear factor kappa B signaling, leukocyte activation, cytokine signaling, lipid and atherosclerosis, toll-like receptor signaling, and inflammasome-associated inflammation. VSMC reclustering revealed contractile VSMCs, PTHLH+ synthetic VSMCs, KRT7+ VSMC-like cells, interferon-responsive VSMCs, pericyte-like mural cells, and osteogenic/modulated VSMCs. Pseudotime analysis showed a broad contractile-to-osteogenic/modulated transcriptional continuum accompanied by increased expression of remodeling-associated genes and selected inflammatory or remodeling-associated receptor genes. CellChat and NicheNet analyses prioritized candidate ligand-receptor and ligand-associated target gene expression patterns involving SPP1-CD44, TNF-TNFRSF1A, IL1B-IL1R1/IL1RAP, MIF-ACKR3, PDGFB-PDGFRB, and FN1-SDC1/ITGB1. In GSE28829, inflammatory macrophage-, osteogenic/modulated VSMC-, candidate ligand-receptor expression-, SPP1-CD44 candidate axis-, and NicheNet-prioritized target program-related signatures were more prominent in advanced plaques and were positively correlated with each other. This integrative transcriptomic analysis identified a highly inflammatory macrophage state and a VSMC remodeling continuum in human atherosclerotic plaques. Candidate ligand-receptor and ligand-associated target gene expression patterns linked inflammatory macrophage activation with osteogenic/modulated VSMC remodeling at the computational level. External bulk data further showed coordinated enrichment of inflammatory and remodeling signatures in advanced plaques. These findings provide a descriptive and hypothesis-generating transcriptomic framework for understanding inflammatory macrophage activation and VSMC remodeling in human atherosclerosis.

atherosclerosis↗

PubMed2004

Classification of arterial plaque by spectral analysis in remodelled human atherosclerotic coronary arteries.

We aimed to characterise and to identify the predominant plaque type in vivo using unprocessed radiofrequency (RF) intravascular ultrasound (US) backscatter, in remodelled segments of human atherosclerotic coronary arteries. A total of 16 remodelled segments were identified using a 30-MHz intravascular ultrasound (IVUS) scanner in vivo. Of these, 9 segments were classified as positively remodelled (>1.05 of the total vessel area in comparison with the proximal and distal reference segments) and 7 as negatively remodelled (<0.95 of reference segment area). Spectral parameters (maximum power, mean power, minimum power and power at 30 MHz) were determined and plaque type was defined as mixed fibrous, calcified or lipid-rich. Positively remodelled segments had a larger total vessel area (16.5 +/- 1.1 mm2 vs. 8.7 +/- 0.9 mm2, p<0.01) and plaque area (7.3 +/- 1.1 mm2 vs. 4.4 +/- 0.8 mm2, p=0.05) than negatively remodelled segments. Both positively and negatively remodelled segments had a greater percentage of fibrous plaque (p<0.01) than calcified or lipid-rich plaque. Comparing positively and negatively remodelled segments, there was no significant difference between the proportion of fibrous, calcified or lipid-rich plaque. We have been able to characterise and to identify plaque composition in vivo in human atherosclerotic coronary arteries. Our data suggest that remodelled segments are predominantly composed of fibrous plaque, as identified by RF analysis, although plaque composition is similar, irrespective of the remodelling type.

Adaptation, Physiological↗

PubMed2001

The influence of plaque orientation (pericardial or myocardial) on coronary arterial remodeling.

BACKGROUND: Many systemic, regional and lesion factors have been identified which may influence arterial remodeling, but little is known about the importance of extravascular resistance to vessel enlargement. As myocardial systolic splinting may significantly affect vessel expansion the effect of plaque orientation on arterial remodeling in eccentric coronary atherosclerotic lesions was examined. METHODS: Using intravascular ultrasound imaging to obtain cross-sectional vessel area (VA), plaque area (PA) and lumen area (LA), remodeling in eccentric left anterior descending coronary artery lesions was compared which predominantly involved the pericardial or free arc (P, n=25) and the myocardial side (M, n=40) of the vessel wall. Normalized vessel area (NVA, VA(lesion)/VA(reference)) was compared as a continuous and categorical variable (positive>1.05, intermediate 0.95-1.05, negative<0.95) as well as remodeling index (RI, VA(lesion)-VA(reference)/PA(lesion)-PA(reference)). RESULTS: The two groups were well matched for clinical and lesion characteristics known to affect remodeling. Reference segments areas were similar in the two groups; while lesion LA was also similar, in the pericardial group there was significantly greater lesion PA (P 12.78+/-0.72, M 10.26+/-0.50 mm(2), P<0.05) and VA (P 15.71+/-0.90, M 12.82+/-0.57 mm(2), P<0.05) demonstrating enhanced compensatory remodeling. Outward remodeling was significantly greater in P than in M by both NVA (P 1.03+/-0.03, M 0.86+/-0.03, P<0.01) and RI (P 0.02+/-0.07, M -1.10+/-0.32, P<0.01). Positive, intermediate and negative remodeling occurred in nine, nine and seven lesions in P and in four, ten and 26 lesions in M (P<0.01). CONCLUSIONS: Remodeling compensates more for plaque growth in eccentric coronary lesions which are surrounded by the pericardium than those surrounded by the myocardium. Extravascular resistance appears to influence arterial remodeling.

Aged↗

PubMed2000

Atherosclerotic arterial remodeling and the localization of macrophages and matrix metalloproteases 1, 2 and 9 in the human coronary artery.

Atherosclerotic luminal narrowing is determined by plaque mass and the mode of geometrical remodeling. Recently, we reported that the type of atherosclerotic remodeling is associated with the presence of histological markers for plaque vulnerability. Inflammation and matrix degrading proteases (MMPs) may play a role in both plaque vulnerability and in expansive arterial remodeling. The aim of the present study was to investigate the association between the remodeling mode and the localization of macrophages and MMPs in coronary atherosclerotic segments. From 36 atherosclerotic coronary arteries, 45 and 51 segments were selected with a vessel area that was >10% smaller and larger compared with the adjacent segments, respectively. No significant difference in staining for macrophages was observed between segments with expansive and constrictive remodeling. More MMP-2 and MMP-9 staining was observed in plaques of expansively remodeled segments compared with constrictively remodeled segments. In general, MMP-staining was less evident in the adventitial layer compared with the plaque. Zymography revealed more active MMP-2 in expansively remodeled segments compared with constrictively remodeled segments (340+/-319 vs. 199+/-181 (adjusted counts/mm(2)), respectively, P=0.019). Zymography did not show differences in inactive MMP-2 or MMP-9 among groups. It might be postulated that MMPs within the plaque play a causal role not only in plaque vulnerability but also in de novo atherosclerotic remodeling.

Aged↗

PubMed2001

Arterial remodeling influences the development of intimal hyperplasia after stent implantation.

OBJECTIVES: We examined whether preinterventional arterial remodeling influenced the interventional results after stenting. BACKGROUND: Arterial remodeling is seen in atherosclerotic lesions, and it may play an important role in the early stage of atherosclerosis. METHODS: We examined 113 lesions that underwent elective stenting using tubular slotted stents under intravascular ultrasound guidance. The lesions were divided into three groups--adequate, intermediate and inadequate remodeling group--according to preinterventional arterial remodeling. The patients were subjected to coronary angiography and intravascular ultrasound evaluation on average 6.4 months after stenting. RESULTS: At baseline and immediately after stenting, there were no differences in quantitative angiographic analysis among remodeling groups. However, the plaque cross-sectional area (CSA) in the minimal lumen CSA at preintervention and intimal hyperplasia CSA at follow-up were significantly larger in the adequate remodeling group than in the inadequate remodeling group. The restenosis rate of stenting for the lesions with inadequate arterial remodeling was very low (9.4%). A significant positive correlation was found between preinterventional plaque CSA and intimal hyperplasia CSA at follow-up (r = 0.47, p < 0.0001). Moreover, remodeling index significantly correlated with relative intimal hyperplasia CSA (r = 0.28, p < 0.01). CONCLUSIONS: Preinterventional arterial remodeling influenced the development of intimal hyperplasia after stenting.

Aged↗

PubMed2001

Impact of coronary artery remodeling on clinical presentation of coronary artery disease: an intravascular ultrasound study.

OBJECTIVES: We examined the association between the features of the culprit lesion in coronary artery disease (CAD) and clinical presentation as shown by intravascular ultrasound (IVUS). BACKGROUND: The association between coronary remodeling pattern and clinical presentation of CAD is unclear. METHODS: We analyzed 125 selected patients who underwent preintervention IVUS. Acute myocardial infarction (AMI) and unstable angina pectoris (UAP) were categorized as an acute coronary syndrome (ACS), and stable angina pectoris (SAP) and old myocardial infarction (OMI) as stable CAD. Coronary remodeling patterns and plaque morphology of the culprit lesion obtained by IVUS were analyzed in terms of their association with clinical presentation or angiographic morphology. RESULTS: Angiographically complex lesions were associated with ACS and OMI. In patients with a complex lesion, positive remodeling was observed more frequently than in those with a simple lesion. In AMI and UAP, positive remodeling was observed more frequently than in SAP and OMI (82% vs. 78% vs. 33% vs. 40%, respectively, p < 0.0001). The remodeling ratio was greater in AMI and UAP than in SAP and OMI (1.26 +/- 0.15 vs. 1.11 +/- 0.10 vs. 0.94 +/- 0.11 vs. 0.96 +/- 0.13, respectively, p < 0.0001). Furthermore, within ACS, the remodeling ratio was greater in AMI than in UAP (1.26 +/- 0.15 vs. 1.11 +/- 0.10, respectively, p < 0.05), whereas the frequency of positive remodeling was not different. CONCLUSIONS: Positive remodeling was more frequently observed in ACS than in stable CAD. Moreover, the degree of positive remodeling was greater in AMI than in UAP. These results may reflect the impact of remodeling types and its degree in the culprit lesion of CAD on clinical presentation.

Adult↗

PubMed2000

Fibrosis and airway remodelling.

The term 'airway remodelling' is now widely used to refer to the development of specific structural changes in the airway wall in asthma. Particular interest has focused on subepithelial fibrosis, myofibroblast accumulation, airway smooth muscle hyperplasia and hypertrophy, mucous gland and goblet cell hyperplasia, and epithelial disruption. The presence of these features is generally accepted, but further studies are still required to define the changes occurring more precisely at the pathological and ultrastructural levels. Attention also needs to be directed towards the existence of such changes in small airways. The natural history of the response has not been well described: remodelling is present in the airways of asthmatic children and of adults with newly diagnosed asthma, and studies that have attempted to relate the extent of remodelling to disease severity have produced conflicting findings. The role of remodelling in the progressive decline in lung function leading to fixed airflow obstruction seen in some patients is also unclear. Epidemiological studies are currently hindered by the absence of a useful non-invasive marker of remodelling. Airway remodelling is frequently assumed to be a consequence of chronic inflammation, but the precise relation between the remodelling and inflammatory components in asthma is unclear. The cellular and molecular events underlying the remodelling process are also poorly understood. There is therefore a need for the development and characterization of animal models that will allow these issues to be explored. Finally, the ability of currently available anti-asthma therapies to prevent or reverse airway remodelling is uncertain. There is some evidence that early treatment with inhaled corticosteroids can lead to improved outcome in asthma but this needs confirmation. Studies addressing the ability of corticosteroid treatment to reverse established structural changes have not produced consistent findings, and there is little information with regard to other therapies such as theophylline and antileukotriene agents. Effective treatment of airway remodelling may require the development of novel therapies directed against appropriate targets.

Animals↗